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Biomedical subjects

R Mathew

Publications and source records attributed to R Mathew.

32 records · Page 2Linked to original sources

Idiopathic atrial flutter in infancy: a review of eight cases.

The experience of three institutions in the management of atrial flutter in infants under 2 years of age without associated heart disease is reviewed. Five babies with neonatal onset were treated with digoxin and had uncomplicated resolution of their arrhythmia, although one continued to have episodes of paroxysmal supraventricular tachycardia for six years. Two of the three older infants required DC cardioversion for complications after quinidine was substituted for digoxin therapy. Digoxin continues to be the preferred initial therapy for non-acutely ill patients; those showing signs of cardiac decompensation should be converted with DC countershock.

Atrial Flutter

Cardiac function in total anomalous pulmonary venous return before and after surgery.

Cardiac performance was evaluated in 12 infants with isolated total anomalous pulmonary venous return. Four had significant pulmonary venous obstruction and severe pulmonary hypertension (group A). Eight had no obvious venous obstruction, and the pulmonary pressures were lower (group B). In all subjects, right ventricular end-diastolic volume was increased (197% of predicted normal) and its ejection fraction was normal. Left ventricular volume was, generally speaking, still in the normal range (87% of predicted normal); however, its ejection fraction was reduced (0.57 vs normal of 0.73) and left ventricular output was low (3.08 L/min/m2 vs normal of 3.98). Left atrial volume was consistently small (53% of predicted normal) with an appendage of normal size. The infants in group A had smaller chamber volumes/m2 BSA than those in group B. Left atrial function was abnormal, characterized by reduced reservoir function and a greater role as "conduit" from right atrium to left ventricle. Left atrial size was not found to be critical in the surgical repair of TAPVR. Cardiac function is restored to normal following surgery.

Angiocardiography

Right ventricular mass estimation by angioechocardiography.

A combined angiocardiographic-echocardiographic method for estimating right ventricular wall mass is described. Biplane cineangiocardiograms are analyzed for ventricular volume in end-diastole, and wall thickness is determined from echocardiograms obtained with a high frequency transducer and strip chart recorder, The intracavitary and the external surface volumes of the ventricle are derived, and the difference multiplied by 1.050, the specific gravity of myocardium. Excellent correlation was observed between right ventricular wall mass and body surface area in normal children (r = 0.93). The mean right ventricular mass was 44.5 g/M2 as compared to 78.1 g/M2 for the left ventricle, corresponding mass/EDV values were 0.48 g/cm3 and 1.26 g/cm3, respectively. In isolated right ventricular pressure overload, the increase in right ventricular mass is chiefly due to the increase in wall thickness; in volume overload, it is due mostly to the increase in chamber volume,

Adolescent

Comparative response of right and left ventricles to volume overload.

The cardiac volume data of 49 normal children were compared with those of 23 with secundum atrial septal defect and 24 with patent ductus arteriosus. Significantly smaller ventricular end-diastolic volumes were observed in the normal infants than in older children (right ventricle 53.9 versus 75.5 cm3/m2; left ventricle 46.7 versus 63.6 cm3/m2). "Distensibility" of the right ventricle (DRV), left ventricle (DLV) and left atrium increased normally with age. DRV and DLV were similar shortly after birth; thereafter, DRV increased more rapidly than DLV (mean DRV 12.7; mean DLV 7.8 cm3/m2 per mm Hg, P less than 0.001). In both atrial septal defect and patent ductus arteriosus, the ipsilateral (involved) ventricles had increased volume, increased output, normal ejection fraction and increased distensibility. The contralateral (left) ventricle in atrial septal defect was smaller than normal (39.6 versus 49.7 cm3, P less than 0.001), and had a smaller ejection fraction (0.63 versus 0.71, P less than 0.01) and output (3.70 versus 4.57 liters/min per m2, P less than 0.005). In contrast, the contralateral (right) ventricle in patent ductus arteriosus remained normal. Left atrial maximal volume was larger than normal in atrial septal defect (46.6 versus 35.9 cm3/m2, P less than 0.001). The left atrial and left ventricular volumes in patent ductus arteriosus were, respectively, 152 and 142 percent of normal, indicating comparable response to the volume load. The left head changes in atrial septal defect may be related both to a functionally restrictive defect and to the difference in distensibility of the ventricles.

Adolescent

Hemodynamics and annuloplasty in isolated mitral regurgitation in children.

Isolated mitral insufficiency in children is quantitated angiographically by comparing the stroke volumes of the right ventricle and left ventricle. The disease results in greater enlargement of the left atrium than of the left ventricle and is accompanied by a significant increase in left atrial "distensibility." Right and left heart pressures may be normal or may be increased; they tend to be elevated in the group with regurgitant fractions of over 50%. Annuloplasty results in marked clinical and hemodynamic improvement and may even be corrective.

Adolescent

Right juxtaposition of the atrial appendages.

We present an infant with right-sided juxtaposition of atrial appendages who had open heart surgery for ventricular septal defect and patent ductus arteriosus. Of 12 cases thus far reported, ventricular d-loop was observed in nine, and normal position of great vessels in four. Contrary to previous views, this condition may not be accompanied by severe conotruncal anomalies.

Adolescent

Effect of verapamil on monocrotaline-induced pulmonary artery hypertension and endothelial cell dysfunction in rats.

Verapamil, a calcium channel blocker has been used with partial success in cases of primary pulmonary hypertension, as well as to reduce hypoxia-induced pulmonary hypertension (PH) in rats. However, its effect on monocrotaline (MCT)-induced PH in rats is not known. We studied the effect of verapamil on MCT-induced PH. Three weeks after a single injection of MCT, significant PH was noted in the MCT-injected rats compared with control (44.35 +/- 3.5 vs. 22 +/- 2.5 mmHg). MCT-injected rats on daily verapamil showed significant reduction in PH (31.5 +/- 3.4 mmHg). The main pulmonary artery of MCT-injected rats revealed subendothelial thickening, thinning and fragmentation of elastic laminae, smooth muscle cell hypertrophy and necrosis or loss of smooth muscle cells, and increased amounts of collagen in media and adventitia. In contrast, the main pulmonary artery of MCT + VP-treated rats showed less intimal thickening, some smooth muscle cell hypertrophy, but little necrosis or loss of cells in addition to disappearance of outer elastic laminae. Smaller pulmonary arteries (less than 150 microns in diameter) in MCT + VP-treated rats showed less medial thickening than MCT groups. However, diminished lung angiotensin-converting enzyme activity suggestive of endothelial cell dysfunction was noted in both MCT and MCT + VP-treated rats. This study indicates that verapamil attenuates MCT-induced PH, but has no effect on pulmonary endothelial cell dysfunction.

Animals

The role of magnesium in lung diseases: asthma, allergy and pulmonary hypertension.

Magnesium is the fourth most abundant metal found in the body. It plays a crucial role in numerous biological processes. It is a natural calcium blocker. It can block or compete with Ca2+ at voltage-dependent, receptor- or leak-operated channels and result in translocation of intracellular Ca2+. Mg2+ inhibits Ca2+ release from the sarcoplasmic reticulum. Intracellular Mg2+ is thought to modulate smooth muscle contractions and the rate of relaxation. Mg2+ is a cofactor of numerous enzymes and is coupled with cellular use of phosphate as an activator and energy source. cAMP-dependent protein and adenylate cyclase are among many enzymes that require Mg2+ for their function. Mg2+ has been used successfully in treating asthma. There is experimental evidence that Mg2+ is required for various immune responses, and in rats, Mg2+ treatment has been shown to attenuate chemically induced pulmonary hypertension. It is not clear if Mg2+ deficiency plays a role in development of some of these diseases, but Mg2+ salts appear to have therapeutic value and certainly it has a role as an adjunct to traditional therapy in various lung diseases.

Animals

Physiology and pathophysiology of pulmonary circulation.

The lungs provide not only respiratory function, but also are involved in metabolism and maintaining homeostasis. The lungs receive the entire cardiac output, circulating blood cells and hormones. The metabolically active vascular endothelial cell lining participates in degrading and synthesizing various hormones and vasoactive substances which affect the pulmonary as well as systemic circulation. The normal state is maintained through complex interaction of the circulating hormones, maturation of the system, the physiological state of the lung cells and metabolism. Any noxious stimulus can disrupt this delicate balance and adversely affect the metabolism of various substances, thus producing an abnormal state. In this review, some of these factors including therapeutic implications are discussed.

Animals

Pulmonary vasculature in monocrotaline-induced hypertensive rats on magnesium therapy.

We have previously demonstrated that magnesium therapy attenuates monocrotaline-induced pulmonary hypertension and right ventricular hypertrophy in rats. In this report we evaluate the effect of oral magnesium therapy on the pulmonary vasculature of monocrotaline-treated rats. Lung sections were prepared for light microscopic examination, and the medial wall thickness of pulmonary arteries of less than 100 microns in diameter was measured. The mean medial wall thickness of control rats was 6.98 +/- 1.16% of the external diameter of the pulmonary artery, the monocrotaline group had a significant increase in medial wall thickness (14.61 +/- 1.52%, p less than 0.005 vs control); in contrast 75% of MCT + magnesium group revealed a significant reduction in medial wall thickness (8.13 +/- 1.26%, p less than 0.02, vs monocrotaline group). Magnesium therapy alone had no effects on pulmonary vasculature. We conclude that magnesium has significant beneficial effects on monocrotaline-induced pulmonary hypertension and the accompanying vascular lesions.

Animals